Comparing the tissue expression patterns of 85 postmenopausal EC patients with healthy hyperplastic endometrium patients, immunohistochemistry and qPCR methods, results showed that the retention of progesterone receptors/ ERα/Erβ (estrogen receptor subtype) and the loss of AR might promote the uncontrolled growth of high-grade endometrial carcinoma (HGEC) [118], suggested that AR deletion was important for HGEC cell proliferation. This evidence concerns the gene ESR1 and endometrial carcinoma.